Early pathogenesis of Yersinia ruckeri infections in rainbow trout (Oncorhynchus mykiss, Walbaum)

摘要: Yersinia ruckeri is the causative agent of yersiniosis or enteric redmouth disease (ERM) and causes significant losses in salmonid aquaculture worldwide. Although infection with this has been reported other fish species, salmonids especially rainbow trout are most susceptible to ERM. Vaccination a commercial Y. bacterin provides good levels protection, however, outbreaks do occur from time time. The understanding how pathogen crucial order develop new preventive therapeutic approaches. aim thesis was study early pathogenesis infections, emphasis on identification portal entry investigation different traits vitro that have associated bacterial virulence. The General Introduction gives an overview micro-organism, ruckeri, it causes. From review clear only little information available about ruckeri. Only recently, mechanisms by which started be unravelled. In first experimental study, its tissue distribution at intervals were investigated using immersion model trout. This strongly mimics natural way therefore, suitable infectious diseases fish. Additional infections carried out determine whether related differences Bacteriological histological examination revealed presence high numbers bacteria gills immediately after infection. Many found attached gill mucus some detected within capillaries between 0 2.5 h post (p.i.). indicates adhere thereafter invade branchial vasculature leading colonization internal organs. These findings show important entry. Nevertheless, virulent strain able survive multiply host, causing septicaemia death several days whereas exposure avirulent strains resulted complete removal could indicate immune evasion major virulence property second interactions gut determined standardized perfusion model. For purpose, perfused explants inoculated for 1 thereafter, processed bacteriological, immunohistochemical demonstration adherence. time, both models also used invasion. Therefore, fluid efferent arch during organ bath following examined bacteriologically. A non-invasive Escherichia coli included as negative control In models, highly adhered not observed. Bacteria seen mucus, epithelium invaded lamina propria gills. observed crypts, villi epithelial layer gut. Few intestinal mucosae. Our results showed E. isolated model, respectively. colonize intestine Significant adherence invasive capacity strains. third compared strains, including adhesion cell lines, invasion intracellular survival lines serum resistance. further characterized selected isolates trout, majority demonstrated significantly lower adhesion. decrease capability treatment sodium metaperiodate proteolytic enzymes suggested carbohydrates well proteins play role consequently, lectins may involved All CHSE-214, FHM R1 cells. One three moderately adhesive invasive. internalization inhibited colchicine cytochalasin-D, suggesting involvement microtubules microfilaments. Monodansylcadaverine never formation clathrin-coated pits receptor-mediated endocytosis role. all assays viable cells 6 inoculation. suggests inside cultured remains intracellularly short period. Analysis susceptibility bactericidal effect resistant, generally sensitive. Taken together, resistance seems correlated vivo Discussion, studies discussed hypothetical proposed relation known factors Finally, perspectives given these contribute prevention conclusion, identified possible portals shown non-phagocytic involve bind specific carbohydrate structures host surfaces. Invasion appears microtubule microfilament dependent process. Virulence probably complex combination capacity, still needs determined.